Electrophysiological correlates of cardiac sarcoidosis: an appraisal of current evidence.

Cardiac sarcoidosis is an underdiagnosed condition that may be present in as many as 25% of patients with systemic sarcoidosis. It is associated with significant morbidity and mortality in affected individuals. The presentation of cardiac involvement in sarcoidosis includes sudden death in the absence of preceding symptoms, conduction disturbances, ventricular arrhythmias, and heart failure. A scarcity of randomized data and a lack of prospective trials underlies the contention between experts on the most appropriate strategies for diagnosis and therapy. This review focuses on the electrophysiological sequelae of the disease, with an emphasis on current diagnostic guidelines, multimodality imaging for early detection, and the role of various therapeutic interventions. Multicentre collaboration is necessary to address the numerous unanswered questions pertaining to management of this disease.

Ventricular arrhythmias from the coronary venous system: Prevalence, mapping, and ablation.

BACKGROUND: The coronary venous system (CVS) is linked to the origin of idiopathic epicardial ventricular arrhythmias (VAs). OBJECTIVE: The purpose of this study was to identify the prevalence and effective mapping/ablation strategies for idiopathic VAs mapped to the CVS. METHODS: Detailed activation and pace-mapping of the right ventricle (RV), left ventricle (LV), CVS, and aortic cusps was performed, followed by attempted catheter ablation. RESULTS: Forty-seven of 511 patients with non-scar-related VAs (21 males, age 55 ± 15) had earliest activation in the CVS, 39 ± 18 ms before QRS. Twenty-five (53%) were in the great cardiac vein, 19 (40%) in the anterior interventricular vein, and 3 (7%) in the middle cardiac vein. We ablated inside CVS in 32 patients (68%) at the earliest activation site, in 18 patients at an adjacent CVS site, and in 14 patients because of an inability to advance the catheter in 4, inadequate power delivery in 2, and for safer distance from the coronary artery in 8. Proximity to coronaries precluded ablation inside the CVS in the remaining 15 patients (32%), who underwent ablation from adjacent left sinus of Valsalva, RV or LV endocardium, or LV epicardium. Success was achieved in 17 of 18 (94%) ablated at the earliest CVS site and in 16 of 29 (55%) ablated at adjacent CVS or non-CVS sites. CONCLUSION: Idiopathic VAs are occasionally (9%) linked to CVS. Although ablation at the earliest CVS site is effective, it is often (62%) precluded, mainly because of proximity to coronary arteries. Ablation at adjacent CVS and non-CVS sites can be successful in 55% of these anatomically challenging cases, for an overall ablation success rate of 70%.

Percutaneous epicardial ablation of ventricular arrhythmias arising from the left ventricular summit: outcomes and electrocardiogram correlates of success.

BACKGROUND: Percutaneous epicardial ablation of ventricular arrhythmias arising from the left ventricular summit is limited by the presence of major coronary vessels and epicardial fat. We report the outcomes of percutaneous epicardial mapping and ablation of ventricular arrhythmias arising from the left ventricular summit and the ECG features associated with successful ablation. METHODS AND RESULTS: Between January 2003 and December 2012, a total of 23 consecutive patients (49 ± 14 years; 39% men) with ventricular arrhythmias arising from the left ventricular summit underwent percutaneous epicardial instrumentation for mapping and ablation because of unsuccessful ablation from the coronary venous system and multiple endocardial LV/right ventricular sites. Successful epicardial ablation was achieved in 5 (22%) patients. In the remaining 18 (78%) cases, ablation was aborted for either close proximity to major coronary arteries or poor energy delivery over epicardial fat. The Q-wave amplitude ratio in aVL/aVR was higher in the successful group, with a ratio of > 1.85 present in 4 (80%) patients in the successful group versus 2 (11%) in the unsuccessful group (P = 0.008). The ratio of R/S wave in V1 was greater in the successful group, with 4 (80%) patients in the successful group having a R/S ratio of > 2 in V1 versus 5 (28%) in the unsuccessful group (P = 0.056). None of the patients in the successful group had an initial q wave in lead V1, as opposed to 6 (33%) in the unsuccessful group. The presence of at least 2 of the 3 ECG criteria above predicted successful ablation with 100% sensitivity and 72% specificity. CONCLUSIONS: Epicardial instrumentation for mapping and ablation of ventricular arrhythmias arising from the left ventricular summit is successful only in a minority of patients because of close proximity to major coronary arteries and epicardial fat. A Q-wave ratio of > 1.85 in aVL/aVR, a R/S ratio of > 2 in V1, and absence of q waves in lead V1 help identify appropriate candidates for epicardial ablation.

Acute hemodynamic decompensation during catheter ablation of scar-related ventricular tachycardia: incidence, predictors, and impact on mortality.

BACKGROUND: The occurrence of periprocedural acute hemodynamic decompensation (AHD) in patients undergoing radiofrequency catheter ablation of scar-related ventricular tachycardia (VT) has not been previously investigated. METHODS AND RESULTS: We identified univariate predictors of periprocedural AHD in 193 consecutive patients undergoing radiofrequency catheter ablation of scar-related VT. AHD was defined as persistent hypotension despite vasopressors and requiring mechanical support or procedure discontinuation. AHD occurred in 22 (11%) patients. Compared with the rest of the population, patients with AHD were older (68.5±10.7 versus 61.6±15.0 years; P=0.037); had a higher prevalence of diabetes mellitus (36% versus 18%; P=0.045), ischemic cardiomyopathy (86% versus 52%; P=0.002), chronic obstructive pulmonary disease (41% versus 13%; P=0.001), and VT storm (77% versus 43%; P=0.002); had more severe heart failure (New York Heart Association class III/IV: 55% versus 15%, P<0.001; left ventricular ejection fraction: 26±10% versus 36±16%, P=0.003); and more often received periprocedural general anesthesia (59% versus 29%; P=0.004). At 21±7 months follow-up, the mortality rate was higher in the AHD group compared with the rest of the population (50% versus 11%, log-rank P<0.001). CONCLUSIONS: AHD occurs in 11% of patients undergoing radiofrequency catheter ablation of scar-related VT and is associated with increased risk of mortality over follow-up. AHD may be predicted by clinical factors, including advanced age, ischemic cardiomyopathy, more severe heart failure status (New York Heart Association class III/IV, lower ejection fraction), associated comorbidities (diabetes mellitus and chronic obstructive pulmonary disease), presentation with VT storm, and use of general anesthesia.

Electrophysiologic findings and long-term outcomes in patients undergoing third or more catheter ablation procedures for atrial fibrillation.

INTRODUCTION: Pulmonary vein (PV) status, arrhythmia sources, and outcomes with ≥3 ablation procedures have not been characterized. METHODS AND RESULTS: All patients with ≥3 procedures were included and underwent antral reisolation of reconnected PVs and ablation of non-PV triggers. Of 2,886 patients who underwent PVI, 181 (6%) had more than 2 ablation procedures (3 procedures in 146 and ≥4 procedures in 35). In 12 patients, the clinical arrhythmia was other than AF. Of the remaining 169 patients, 69 (41%) had 4 reconnected PVs, 27 (16%) had 3, 31 (18%) had 2, and 29 (17%) had 1. Only 13 (8%) had all PVs still isolated. Provocative techniques in 127 patients initiated PV triggers in 92 patients, including AF or PV atrial tachycardia in 64 (50%), and reproducible PV APDs in 28 (22%). Thirty-six (20%) had a new non-PV trigger targeted. At a mean of 36 months (12-119 months) after last procedure, 63 patients (47%) had no AF off antiarrhythmic drugs (AAD); 28 (21%) had no AF with AAD; and 18 (13%) had rare AF with good symptom control; 26 patients (19%) had recurrent AF. CONCLUSIONS: At time of third or greater AF ablation, PV reconnection is the rule (92%) and PV triggers initiating AF can be demonstrated. Following repeat PVI and targeting non-PV triggers, 81% of patients had clinical AF control. Our findings suggest that PV reisolation and attempts to identify and eliminate non-PV triggers are effective and support the role of multiple repeat procedures for AF recurrence.

Idiopathic ventricular arrhythmias originating from the moderator band: Electrocardiographic characteristics and treatment by catheter ablation.

BACKGROUND: The moderator band (MB) can be a source of premature ventricular contractions (PVCs), monomorphic ventricular tachycardia (VT), and idiopathic ventricular fibrillation (IVF). OBJECTIVE: The purpose of this study was to define the electrocardiographic (ECG) characteristics and procedural techniques to successfully identify and ablate MB PVCs/VT. METHODS: In 10 patients with left bundle branch block morphology PVCs/VT, electroanatomic mapping in conjunction with intracardiac echocardiography (ICE) localized the site of origin of the PVCs to the MB. Clinical characteristics of the patients, ECG features, and procedural data were collected and analyzed. RESULTS: Seven patients presented with IVF and 3 presented with monomorphic VT. In all patients, the ventricular arrhythmias (VAs) had a left bundle branch block QRS with a late precordial transition (>V4), a rapid downstroke of the QRS in the precordial leads, and a left superior frontal plane axis. Mean QRS duration was 152.7 ± 15.2 ms. Six patients required a repeat procedure. After mean follow-up of 21.5 ± 11.6 months, all patients were free of sustained VAs, with only 1 patient requiring antiarrhythmic drug therapy and 1 patient having isolated PVCs no longer inducing VF. There were no procedural complications. CONCLUSION: VAs originating from the MB have a distinctive morphology and often are associated with PVC-induced ventricular fibrillation. Catheter ablation can be safely performed and is facilitated by ICE imaging.

Appropriateness of primary prevention implantable cardioverter-defibrillators at the time of generator replacement: are indications still met?

OBJECTIVES: This study sought to determine how often patients with primary prevention implantable cardioverter-defibrillators (ICDs) meet guideline-derived indications at the time of generator replacement. BACKGROUND: Professional societies have developed guideline criteria for the appropriate implantation of an ICD for the primary prevention of sudden cardiac death. It is unknown whether patients continue to meet criteria when their devices need replacement for battery depletion. METHODS: We performed a retrospective chart review of patients undergoing replacement of primary prevention ICDs at 2 tertiary Veterans Affairs Medical Centers. Indications for continued ICD therapy at the time of generator replacement included a left ventricular ejection fraction (LVEF) ≤35% or receipt of appropriate device therapy. RESULTS: In our cohort of 231 patients, 59 (26%) no longer met guideline-driven indications for an ICD at the time of generator replacement. An additional 79 patients (34%) had not received any appropriate ICD therapies and had not undergone reassessment of their LVEF. Patients with an initial LVEF of 30% to 35% were less likely to meet indications for ICD therapy at the time of replacement (odds ratio: 0.52; 95% confidence interval: 0.30 to 0.88; p = 0.01). Patients without ICD indications subsequently received appropriate ICD therapies at a significantly lower rate than patients with indications (2.8% vs. 10.7% annually, p < 0.001). If ICD generator explantations were performed instead of replacements in the patients without ICD indications, the cost savings would be $1.6 million. CONCLUSIONS: Approximately 25% of patients who receive primary prevention ICDs may no longer meet guideline indications for ICD use at the time of generator replacement, and these patients receive subsequent ICD therapies at a significantly lower rate.

Scar progression in patients with nonischemic cardiomyopathy and ventricular arrhythmias.

BACKGROUND: Disease progression in patients with nonischemic cardiomyopathy (NICM) is poorly understood. OBJECTIVE: To assess left ventricular (LV) scar progression and dilatation by using endocardial electroanatomic mapping. METHODS: We studied 13 patients with NICM and recurrent ventricular tachycardia. Two detailed sinus rhythm endocardial voltage maps (265 ± 122 points/map) were obtained after a mean of 32 months (range 9-77 months). The scar area, defined by low bipolar (BI; <1.5 mV) and unipolar (UNI; <8.3 mV) endocardial voltage, and the LV volume were measured and compared. A scar difference of >6% of the LV surface and an increase in LV volume of ≥20 mL were considered beyond measurement error. RESULTS: Six (46%) patients had an increase in scar area beyond boundaries of prior ablation. Five patients had an increase in UNI and 1 patient had an increase in both BI and UNI areas. The increase in BI area represented 16% and the increase in UNI area represented 6.5%-46.2% of the LV surface. A significant decrease in LV ejection fraction was found only in patients with scar progression (from 39% ± 8% to 32% ± 8%; P = .003). LV dilation (LV volume increase ranging between 9% and 23%) was noted in 3 patients, all of whom had scar progression. CONCLUSIONS: Progressive scarring with an increase in the area of UNI and less commonly BI electrogram abnormality is seen in 46% of the patients with NICM and ventricular tachycardia and is associated with LV dilatation and decrease in LV ejection fraction. The prominent UNI abnormality suggests predominantly midmyocardial or epicardial scarring.

Risk of stroke or transient ischemic attack after atrial fibrillation ablation with oral anticoagulant use guided by ECG monitoring and pulse assessment.

INTRODUCTION: We sought to gain insight into stroke risk after atrial fibrillation (AF) ablation. METHODS AND RESULTS: We followed 1,990 patients for >1 year (49 ± 29 months) who underwent AF ablation. Prior to stopping oral anticoagulants (OAC), we performed 3-week transtelephonic ECG monitoring (TTM) and taught patients heart rate and pulse assessment. Documented AF or inability to do monitoring or assess pulse precluded stopping OAC in CHADS2 ≥1 patients. OAC was stopped in 546/840 (65%) with CHADS2  = 0; 384/796 (48%) with CHADS2  = 1 and 101/354 (40%) with CHADS2 ≥ 2. Sixteen strokes or TIAs occurred (0.2%/patient-year); 5 in CHADS2  = 0 patients (all off OAC); 5 in CHADS2  = 1 (1 off and 4 on OAC); and 6 in CHADS2 ≥2 (2 off and 4 on OAC). Twelve of 16 patients (75%) with stroke or TIA had documented AF. In patients "off " OAC, stroke rate/year stratified by the CHADS2 score was similar (CHADS2  = 0: 0.28%; CHADS2  = 1: 0.07%; CHADS2 ≥2: 0.50%; P = NS). There was no difference in stroke risk "on" versus "off " OAC in CHADS2  = 1 (0.48% vs. 0.07%) or CHADS2 ≥2 (0.39% vs. 0.50%). Risk of major bleeding per patient year "on" OAC was > "off " OAC (13/1,138 (1.14%) versus 1/832 (0.1%); P<0.016). CONCLUSIONS: Post-AF ablation with OAC guided by TTM and pulse assessment: (1) Overall stroke or TIA rate risk is low and risk is due to recurrent AF and (2) OAC can be stopped in 40% of CHADS2 ≥2 patients with low stroke and hemorrhagic risk.

Catheter ablation of ventricular fibrillation: importance of left ventricular outflow tract and papillary muscle triggers.

BACKGROUND: Monomorphic ventricular premature depolarizations (VPDs) have been found to initiate ventricular fibrillation (VF) or polymorphic ventricular tachycardia (PMVT) in patients with and without structural heart disease. OBJECTIVE: The purpose of this study was to describe and characterize sites of origin of VPDs triggering VF and PMVT. METHODS: The distribution of mapping-confirmed VPDs, electrophysiology laboratory findings, and results of radiofrequency catheter ablation were analyzed. RESULTS: Among 1132 consecutive patients who underwent ablation for ventricular arrhythmias, 30 patients (2.7%) with documented VF/PMVT initiation were identified. In 21 patients, VF/PMVT occurred in the setting of cardiomyopathy; in 9 patients, VF/PMVT was idiopathic. The origin of VPD trigger was from the Purkinje network in 9, papillary muscles in 8, left ventricular outflow tract in 9, and other low-voltage areas unrelated to Purkinje activity in 4. Each distinct anatomic area of origin was associated with VF/PMVT triggers in patients with and without heart disease. Acute VPD elimination was achieved in 26 patients (87%), with a decrease in VPDs in another 3 patients (97%). During median follow-up of 418 days (interquartile range [IQR] 144-866), 5 patients developed a VF/PMVT recurrence after a median of 34 days (IQR 1-259). Rare recurrence was noted in patients with and without structural disease and from each distinct anatomic origin. The total burden of VF/PMVT episodes/shocks was reduced from a median of 9 (IQR 2.5-22.5) in the 3 months before ablation to 0 (IQR 0-0, total range 0-2) during follow-up (P <.0001). CONCLUSION: Catheter ablation of VPD-triggered VF/PMVT is highly successful. Left ventricular outflow tract and papillary muscles are common and are previously unrecognized sites of origin of these triggers in patients with and without structural heart disease.

Unipolar voltage abnormality is associated with greater left ventricular dysfunction in ischemic cardiomyopathy.

INTRODUCTION: Following myocardial infarction (MI), left ventricular function is determined by cardiac remodeling occurring in both infarcted and noninfarcted myocardium (NIM). Unipolar voltage mapping may detect remodeling changes in NIM that are associated with the left ventricular ejection fraction (LVEF). We aimed to identify (1) unipolar voltage characteristics in patients with chronic MI, and (2) association of voltage abnormalities with degree of left ventricular dysfunction (LVD). METHODS AND RESULTS: Two groups of patients with ischemic cardiomyopathy (ICM) who underwent LV endocardial mapping during catheter ablation for ventricular tachycardia (VT) between January 2010 and December 2012 were studied. The first group (19 males) had mild to moderate LVD (M-LVD, LVEF >35%) and was matched for age, sex, infarction size, and infarction location with 10 males who had severe LVD (S-LVD, LVEF <35%). Both bipolar and unipolar endocardial abnormal voltage areas were measured and compared between groups. Abnormal bipolar area was comparable in both groups (30 ± 8% in the S-LVD group vs 28 ± 8% in the M-LVD group; P = 0.5). Total abnormal unipolar voltage area was significantly larger in the S-LVD group (57 ± 14% vs 43 ± 13%; P = 0.02). The abnormal unipolar voltage area within the normal bipolar voltage area was greater in the S-LVD group (26 ± 11% vs 15 ± 16%; P = 0.03). In receiver operating characteristic curve analysis, an 18.0% cut-off value for abnormal unipolar area within NIM identified severe LVD, with 90% sensitivity and 79% specificity (area under the curve 0.821). CONCLUSIONS: Patients with ICM and severe LVD have larger areas of unipolar voltage abnormality in the noninfarcted tissue than patients with M-LVD.

Assessing arrhythmia burden after catheter ablation of atrial fibrillation using an implantable loop recorder: the ABACUS study.

INTRODUCTION: Arrhythmia monitoring in patients undergoing atrial fibrillation (AF) ablation is challenging. Transtelephonic monitors (TTMs) are cumbersome to use and provide limited temporal assessment. Implantable loop recorders (ILRs) may overcome these limitations. We sought to evaluate the utility of ILRs versus conventional monitoring (CM) in patients undergoing AF ablation. METHODS AND RESULTS: Forty-four patients undergoing AF ablation received ILRs and CM (30-day TTM at discharge and months 5 and 11 postablation). Over the initial 6 months, clinical decisions were made based on CM. Subjects were then randomized for the remaining 6 months to arrhythmia assessment and management by ILR versus CM. The primary endpoint was arrhythmia recurrence. The secondary endpoint was actionable clinical events (change of antiarrhythmic drugs [AADs], anticoagulation, non-AF arrhythmia events, etc.) due to either monitoring strategy. Over the study period, 6 patients withdrew. In the first 6 months, AF recurred in 18 patients (7 noted by CM, 18 by ILR; P = 0.002). Five patients in the CM (28%) and 5 in the ILR arm (25%; P = NS) had AF recurrence during the latter 6 months. AF was falsely diagnosed frequently by ILR (730 of 1,421 episodes; 51%). In more patients in the ILR compared with the CM arm, rate control agents (60% vs 39%, P = 0.02) and AADs (71% vs 44%, P = 0.04) were discontinued. CONCLUSION: In AF ablation patients, ILR can detect more arrhythmias than CM. However, false detection remains a challenge. With adequate oversight, ILRs may be useful in monitoring these patients after ablation.

Inducibility of atrial fibrillation and flutter following pulmonary vein ablation.

INTRODUCTION: Prior reports demonstrate prognostic value in noninducibility of atrial arrhythmias after atrial fibrillation (AF) ablation and suggest their utility in guiding additional ablation lesion sets. The type and mechanism of induced atrial arrhythmias, their relationship to the underlying atrial substrate, and prognostic significance of induced organized atrial arrhythmias are unknown. METHODS AND RESULTS: One hundred forty-four patients (30 women; median age 60 years; 54% with paroxysmal AF) undergoing AF ablation (circumferential pulmonary vein isolation and focal ablation of nonvein triggers on isoproterenol) were evaluated prospectively. All underwent a standardized postablation induction protocol from the coronary sinus and right atrium: 15 beat burst pacing at 250 milliseconds and decrementing to 180 milliseconds. Sustained rhythms were defined as greater than 2 minutes Of 144 patients, 55 patients (38.2%) did not have sustained inducible arrhythmias. Fifty-two (36.1%) had inducible AF and 37 (25.7%) had inducible organized arrhythmias. A logistic regression analysis showed that age (OR 2.10 per decade; P = 0.003) and hypertension (OR 4.15; P = 0.009) were predictive of inducibility. However, inducibility of either AF or organized arrhythmias was not prognostic of clinical recurrence at 1 year postablation (P = 0.65). Furthermore, inducibility of organized arrhythmias did not predict clinical recurrence of an organized arrhythmia. Only LA size (OR 2.18; 95% CI 1.02-4.67; P = 0.04) and persistent AF (OR 2.43; 95% CI 1.09-5.40; P = 0.03) predicted atrial arrhythmia recurrence. CONCLUSIONS: Multisite atrial burst pacing post-AF ablation induced organized rhythms in 25.7% and AF in 36.1% of patients after AF ablation. Hypertension and age predict inducibility of arrhythmias, but inducibility did not predict clinical recurrence in follow-up. Distinguishing organized atrial arrhythmias from AF did not yield any further prognostic information. The utility of aggressive stimulation protocols after AF ablation for prognosis and to guide therapy appears limited.

Efforts to enhance catheter stability improve atrial fibrillation ablation outcome.

BACKGROUND: Contemporary techniques to enhance anatomical detail and catheter contact during atrial fibrillation (AF) ablation include (1) the integration of preacquired tomographic reconstructions with electroanatomical mapping (3-dimensional image integration [I-EAM]), (2) the use of steerable introducers (SIs), and (3) high-frequency jet ventilation (HFJV). OBJECTIVE: To prove that using these stabilizing techniques during AF ablation improves 1-year procedural outcome. METHODS: We studied 300 patients undergoing AF ablation at our institution. Patients were divided into 3 equal treatment groups (100 patients each) on the basis of the tools utilized: (1) group 1: AF ablation performed without I-EAM, SI, or HFJV; (2) group 2: AF ablation performed using I-EAM and SI, but without HFJV; and (3) group 3: AF ablation performed with I-EAM, SI, and HFJV. The primary outcome was freedom from AF 1 year after a single ablation procedure. The burden of both acute and chronic pulmonary vein reconnection was also assessed. RESULTS: Patients from groups 2 and 3 had significantly more nonparoxysmal AF (17% vs 30% vs 39%; P = .002), larger left atria (4.2 ± 0.8 cm vs 4.4 ± 0.7 cm vs 4.5 ± 0.8 cm; P<.001), and higher body mass index (BMI; 28.5 ± 5.8 kg/m² vs 29.1 ± 4.8 kg/m² vs 31.2 ± 5.4 kg/m²; P<.001). Despite these differences, with adoption of I-EAM, SI, and HFJV we noted a significant improvement in 1-year freedom from AF (52% vs 66% vs 74%; P = .006) as well as fewer acute (1.1 ± 1.2 vs 0.9 ± 1.1 vs 0.6 ± 0.9; P = .03) and chronic (3.5 ± 0.9 vs 3.2 ± 0.9 vs 2.4 ± 1.0; P = .02) pulmonary vein reconnections. CONCLUSIONS: The incorporation of contemporary tools to enhance anatomical detail and ablation catheter stability significantly improved 1-year freedom from AF after ablation.

New unipolar electrogram criteria to identify irreversibility of nonischemic left ventricular cardiomyopathy.

OBJECTIVES: This study sought to assess the value of left ventricular (LV) endocardial unipolar electroanatomical mapping (EAM) in identifying irreversibility of LV systolic dysfunction in patients with left ventricular nonischemic cardiomyopathy (LVCM). BACKGROUND: Identifying irreversibility of LVCM would be helpful but cannot be reliably accomplished by bipolar EAM or cardiac magnetic resonance identification of macroscopic scar. METHODS: Detailed endocardial LV EAM was performed in 3 groups: 1) 24 patients with irreversible LVCM (I-LVCM) but with no or minimal macroscopic scar (<15% LV surface) evidenced on bipolar voltage EAM and/or cardiac magnetic resonance; 2) 14 patients with reversible ventricular premature depolarization-mediated LVCM (R-LVCM); and 3) 17 patients with structurally normal hearts. LV endocardial unipolar electrogram amplitude and area of unipolar amplitude abnormality were defined after excluding macroscopic scar. RESULTS: Unipolar amplitude differed in the 3 groups: median of 7.6 (interquartile range [IQR]: 5.5 to 9.7) mV in I-LVCM group, 13.2 (IQR: 10.4 to 16.2) mV in R-LVCM group, and 16.3 (IQR: 13.6 to 19.8) mV in structurally normal hearts group (p < 0.001). Areas of unipolar abnormality represented a large proportion of total LV surface in I-LVCM, 64.7% (IQR: 47.5% to 75.9%) compared with R-LVCM, 5.2% (IQR: 0.0% to 19.1%) and structurally normal hearts, 0.1% (IQR: 0.0% to 0.9%), groups (p < 0.001). A unipolar abnormality area cutoff of 32% of total LV surface was 96% sensitive and 100% specific in identifying irreversible cardiomyopathy among patients with LV dysfunction (I-LVCM and R-LVCM), p < 0.001. CONCLUSIONS: Detailed unipolar voltage mapping can identify irreversible myocardial dysfunction consistent with fibrosis, even in the absence of bipolar EAM or cardiac magnetic resonance abnormalities, and may serve as valuable prognostic tool in patients presenting with LVCM to facilitate clinical decision making.

Risk of stroke and atrial fibrillation after radiofrequency catheter ablation of typical atrial flutter.

BACKGROUND: Studies suggest that 18%-50% of the patients develop atrial fibrillation (AF) after typical atrial flutter (AFL) ablation. However, little data exist about the incidence of and risk factors for stroke and AF after successful ablation of typical AFL. OBJECTIVES: To determine the risk of stroke and AF after radiofrequency ablation of typical AFL. METHODS: A retrospective review of patients undergoing AFL ablation between 2002 and 2010 was performed to determine the incidence of and risk factors for stroke and AF after successful ablation of typical AFL. RESULTS: The study cohort consisted of 126 patients (age 66 ± 10 years) with a mean follow-up of 40 ± 30 months after ablation. Following successful AFL ablation, AF occurred in 46 patients (37%), with an incidence of 104 cases of documented AF per 1000 person-years after AFL ablation. Twenty patients (16%) developed new AF after AFL ablation. Stroke occurred in 8 patients (6%) during follow-up, with an incidence of 21 strokes per 1000 person-years. Six of the 8 patients (75%) with strokes had documented AF occurrences after AFL ablation. The presence of AF after AFL ablation was the only risk factor associated with the risk for future stroke. CONCLUSIONS: Patients with typical AFL undergoing successful ablation are at an elevated risk for AF and stroke following the procedure. Because postprocedure AF is the only identifiable risk factor for stroke, rigorous monitoring of patients after typical AFL may help identify those patients who are at an increased risk for stroke.

Predictors of recovery of left ventricular dysfunction after ablation of frequent ventricular premature depolarizations.

BACKGROUND: Frequent ventricular premature depolarizations (VPDs) can cause reversible left ventricular (LV) dysfunction. However, not all patients normalize their LV function after VPD elimination. OBJECTIVE: To evaluate predictors of recovery of LV function following the elimination of frequent VPDs. METHODS: We identified patients with ≥10% VPDs/24 h and an LV ejection fraction of <50% who underwent successful ablation between 2007 and 2011. Subjects were classified as having reversible (≥10% increase to a final LV ejection fraction of ≥50%) or irreversible (≤10% increase or final LV ejection fraction <50%) LV dysfunction on the basis of echocardiographic follow-up. A reference group with ≥10% VPDs but normal LV function was identified. RESULTS: One hundred fourteen patients with ≥10% VPDs were identified; 66 had preserved and 48 had impaired LV function. Over a median follow-up of 10.6 months, 24 of 48 were classified as reversible and 13 of 48 as irreversible and 11 of 44 were excluded. There was a gradient of VPD QRS duration between the control, reversible, and irreversible groups (mean VPD QRS 135, 158, and 173 ms, respectively; P < .001). This gradient persisted even for the same site of origin. In multivariate analysis, the only independent predictor of irreversible LV function was VPD QRS duration (odds ratio 5.07 [95% confidence interval 1.22-21.01] per 10-ms increase). CONCLUSION: In patients with LV dysfunction and frequent VPDs, we identified VPD QRS duration as the only independent predictor for the recovery of LV function after ablation. This suggests that VPD QRS duration may be a marker for the severity of underlying substrate abnormality.